1149. Organism and Host-Specific Differences in the Interaction Between Human Mannose-Binding Lectin and Staphylococcus aureus
Session: Poster Abstract Session: Innate and Adaptive Immunity to Infections
Saturday, October 22, 2011
Room: Poster Hall B1
  • IDSA POSTER 1149 MBL & SA binding.pdf (790.5 kB)
  • Background: 

    Factors mediating transition from S. aureus colonisation to infection and determinants of complicated S. aureus infection are poorly understood. Binding of mannose binding lectin (MBL), a pattern recognition receptor, to S. aureus enhances phagocytosis but is influenced by the surface glycoprotein repertoire which varies with respect to bacterial lineage. The hypotheses that MBL binding is associated with lineage and that MBL binds less well to invasive isolates, especially those causing complicated infection, were investigated.


    MBL binding to S. aureus, collected from bacteraemic and colonized patients, was measured using single donor serum. MBL levels were measured pre and post incubation with a known quantity of S. aureus. Inter-individual differences in MBL binding were investigated using serum from eight patients. Binding specificity was confirmed. S. aureus isolates were strain typed.  


    70 bacteraemia isolates, from 12 lineages and 59 MRSA colonization isolates, from two lineages (43=CC22, & 16=CC30) were investigated. MBL consumption varied significantly by S. aureus lineage (range 23%-53%, p=0.02). After segregation with respect to lineage, MBL consumption did not differ between invasive and colonizing isolates (CC22 p=0.31, CC30 p=0.73). MBL binding to isolates causing uncomplicated infection was similar to isolates causing death (n=8, p=0.98) or disseminated infection (n=12, p=0.91). Significant inter-individual differences in MBL binding was observed (range 21%-60%, p<0.01). 


    This is the first demonstration of lineage-specific differences in the host immune response to S. aureus. The similarity in MBL binding between colonising and bacteraemia isolates reflects the similar distribution of genetic lineages between these groups. MBL binding was not associated with disease trajectory in S. aureus infection. This is also the first demonstration of inter-individual differences in MBL function. This may be mediated by post-translational modification. In-vivo, glycosylation impairs MBL-mediated complement activation. Whether the immunoparesis seen in diabetes, which causes increased protein glycosylation, is associated with impaired MBL function is under investigation.

    Subject Category: E. Innate and adaptive immunity to infections, including vaccine immunology

    Jonathan Lambourne, MD, PhD1, Richard Holliman, MD, MSc, DSc1,2 and Jodi Lindsay, MSc, PhD1, (1)Centre for Infection, Division of Cellular & Molecular Medicine, St George’s University of London, London, United Kingdom, (2)Department of Microbiology, St George’s Healthcare NHS Trust, London, United Kingdom


    J. Lambourne, None

    R. Holliman, None

    J. Lindsay, None

    Findings in the abstracts are embargoed until 12:01 a.m. EST Thursday, Oct. 20 with the exception of research findings presented at IDSA press conferences.